Many plasticity mechanisms have been characterized in vitro, but little is known about their function in circuits mediating learning. Such mechanisms may not only play a crucial role in normal motor function, but may be deficient in movement disorders such as cerebellar ataxia. To understand these plasticity mechanisms, we are studying their necessity in a simple paradigm, motor learning in the vestibulo-ocular reflex (VOR). Despite the diversity of plasticity mechanisms in the circuit for the VOR, much effort in this field has focused upon the role of a single plasticity mechanism, LTD at the parallel fiber-Purkinje cell (pf-Pk) synapse, in mediating both increases and decreases in the gain of the VOR. However, there is evidence that these oppositely directed changes in VOR gain are mediated by different plasticity mechanisms. Thus, we propose three specific aims to investigate the roles of LTD and LTP at the pf-Pk synapse. 1) Do increases and decreases in VOR gain differentially rely upon pf-Pk LTD? 2) Do increases and decreases in VOR gain differentially rely upon pf-Pk LTP? 3) Do increases and decreases in VOR gain induce different patterns of gene expression in Purkinje cells, or elsewhere in the circuit?